Factors affecting visual outcome and progression of diabetic retinopathy after cataract surgery in type II diabetic patients

Full text

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PROGRESION OF DIABETIC RETINOPATHY

AFTER CATARACT SURGERY IN TYPE II

DIABETIC PATIENTS

Dissertation submitted to

Tamil Nadu Dr. M.G.R. Medical University

Chennai

for

MS (OPHTHALMOLOGY)

April 2011

Govt. Stanley Medical College

Chennai

(2)

This is to certify that this dissertation titled “FACTORS

AFFECTING VISUAL OUTCOME AND PROGRESION OF DIABETIC

RETINOPATHY AFTER CATARACT SURGERY IN TYPE II

DIABETIC PATIENTS ” is the original and bonafide work done by

Dr. Ramya .R under our guidance and supervision at the Government Stanley Medical College & Hospital, Chennai – 600 001, during the

tenure of her course in M.S. Ophthalmology from June - 2008 to

April-2011 held under the regulation of the Tamilnadu Dr. M.G.R.

Medical University, Guindy, Chennai - 600032.

PROF. Dr. P. KUMARAVEL, M.S.D.O.,

Professor and Head

Department of Ophthalmology Government Stanley Medical College

Chennai- 600 001.

PROF. Dr. C. VAMSADHARA., M.D.,Ph.D.,

Dean

Government Stanley Medical College

Chennai- 600 001.

PROF. Dr. K. BASKAR, M.S. D.O., Guide and Unit Chief, Department of Ophthalmology, Govt. Stanley Medical College,

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I am grateful to Prof.Dr.C.Vamsadhara, M.D.,Ph.D, Dean, Government Stanley Medical College for allowing me to do this dissertation.

I express my profound gratitude to Dr.P.Kumaravel ,M.S.,D.O,

Professor and HOD department of Ophthalmology Govt. Stanley Medical College Chennai for providing me all the necessary facilities and guidance to enable me to complete my study.

I am very grateful to Prof. K. Baskar, M.S. D.O., for the guidance and invaluable help rendered at various stages.

I sincerely extend my thanks to Prof. K. Kanmani, M.S., D.O, for his kind support in conducting the study.

I am grateful to Asst. Professors Dr.Srinivasan, M.S.,D.O, Dr.Nandhini M.S., Dr.Venkatesh M.S., Dr.Meenakshi M.S., and

Dr.Geetha,M.S.D.O, for their suggestions in preparation of this study.

I am also thankful to Dr.Madhavan M.D. (Gen.Medicine) Professor and HOD department of Diabetology Govt Stanley Medical College Chennai for his support in carrying out this study.

My sincere thanks to all my fellow post graduates for having helped in every possible way.

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SECTION – I

S.No. Title Page.

No.

1. Introduction 1

2. Pathophysiology of diabetic retinopathy 3

3. Epidemiology of diabetic retinopathy 6

4. Clinical aspects of diabetic retinopathy 8

5. Classification of diabetic retinopathy 10

6. Risk factors for diabetic retinopathy 16

7. Pathogenesis of diabetic cataract 18

8. Studies regarding incidence of diabetic cataract 21

9. Cataract surgery in diabetic patients 24

SECTION – II 10. Aim of study 32

11. Materials and methods 32

12. Inclusion and exclusion criteria 33

13. Procedure 34

14. Analysis 38

15. Results 56

16. Discussion 59

17. Conclusion 65

SECTION – III ANNEXURE

18. Bibliography

19. Proforma

20. Abbreviations

21. Master Chart

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INTRODUCTION

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(7)

PATHOPHYSIOLOGY OF DIABETIC RETINOPATHY

The exact mechanism by which diabetes causes retinopathy remains

unclear, but several theories have been postulated to explain the typical course

and history of the disease.

Platelets and blood viscosity

The variety of hematologic abnormalities seen in diabetes, such as

increased erythrocyte aggregation, decreased red blood cell deformability,

increased platelet aggregation, and adhesion, predispose to sluggish circulation,

endothelial damage, and focal capillary occusion. This leads to retinal

ischemia, which, in turn, contributes to the development of diabetic

retinopathy.

Aldose reductase and vasoproliferative factors

Fundamentally, diabetes mellitus causes abnormal glucose metabolism

as a result of decreased levels or activity of insulin. Increased levels of blood

glucose are thought to have a structural and physiologic effect on retinal

capillaries causing them to be both functionally and anatomically incompetent.

A persistent increase in blood glucose levels shunts excess glucose into

the aldose reductase pathway in certain tissues, which converts sugars into

alcohol (e.g., glucose into sorbitol, galactose to dulcitol). Intramural pericytes

(8)

eventually leading to the loss of its primary function (i.e., auto regulation of

retinal capillaries).

Loss of function of pericytes results in weakness and eventual saccular

out pouching of capillary walls. These microaneurysms are the earliest

detectable signs of diabetic retinopathy.

Increased permeability of these vessels results in leakage of fluid and

proteinaeous material, which clinically appears as retinal thickening and

exudaes. If the swelling and exudation would happen to involve the macula, a

diminution in central vision may be experienced. Macular edema is the most

common cause of vision loss in patients with nonproliferative diabetic

retinopathy.

Another theory to explain the development of macular edema deals with

the increased levels of diacylglycerol from the shunting of excess glucose. This

is thought to activate protein kinase C, which, in turn, affects retinal blood

dynamics, especially permeability and flow, leading to fluid leakage and retinal

thickening.

As the disease progresses, eventual closure of the retinal capillaries

occurs, leading to hypoxia. Infarction of the nerve fiber layer leads to the

formation of cotton-wool spots with associated stasis in axoplasmic flow.

More extensive retinal hypoxia triggers compensatory mechanisms

(9)

abnormalities, such as venous beading, loops, and dilation, signify increasing

hypoxia and almost always are seen bordering the areas of capillary

nonperfusion. Intraretinal microvascular abnormalities represent either new

vessel growth or remodeling of preexisting vessels through endothelial cell

proliferation within the retinal tissues to act as shunts through areas of

nonperfusion.

Further increase in retinal ischemia trigger the production of

vasoproliferative factors that stimulate new vessel formation.

Neovascularization most commonly is observed at the borders of perfused and

nonperfused retina and most commonly occur along the vascular arcades and at

the optic nerve head. The new vessels break through and grow along the

surface of the retina and into the scaffold of the posterior hyaloid face. These

delicate vessels are disrupted easily by vitreous traction, which leads to

hemorrhage into the vitreous cavity or the preretinal space.

These new blood vessels initially are associated with a small amount of

fibroglial tissue formation. However, as the density of the neovascular frond

increases, so does the degree of fibrous tissue formation. In later stages, the

vessels may regress leaving only networks of avascular fibrous tissue adherent

to both the retina and the posterior hyaloids face. As the vitreous contracts, it

may exert tractional forces on the retina via these fibroglial connections.

Traction may cause retinal edema, retinal heterotropia, and both tractional

(10)

EPIDEMIOLOGY OF DIABETIC RETINOPATHY

Frequency

Diabetic retinopathy is emerging as one of the important causes of

blindness in both developing and developed countries. The World Health

Organization has estimated that, the number of adults with diabetes in the

world would increase alarmingly: from 135million in 1995 to 300 million in

2025.

In India, this increase is expected to be the greatest; nearly 195% from

18 million in 1995 to 54 million in 2025.

Studies done by the Indian council of medical research in the early

1970’s had shown the prevalence of diabetes in India to be 2.5% in the urban

population and 1.5% in the rural population. However recent reports have

shown the prevalence to be in the range of 12 to 14% in the urban population.

Of these patients with diabetes, over 20% are expected to be suffering from

diabetic retinopathy. The prevalence of diabetes in the rural population is

expected to be about 5%.

Race

An increased risk of diabetic retinopathy appears to exist in patients with

(11)

Sex

Sex does not appear to have any affect on the development of diabetes

or diabetic retinopathy.

Age

With increasing duration of diabetes, or with increasing age since the

onset of diabetes, there is a higher risk of developing diabetic retinopathy and

the complications of diabetic retinopathy, including diabetic macular edema

(12)

CLINICAL ASPECTS OF DIABETIC RETINOPATHY

History

In the initial stages, patients are generally asymptomatic; however, in

the more advanced stages of the disease, patients may experience symptoms,

including blurred vision, distortion, or visual acuity loss.

Examination

Microaneurysms

o Earliest clinical sign of diabetic retinopathy

o Secondary to capillary wall outpouching due to pericyte loss

o Appear as small red dots in the superficial retinal layers

o Fibrin and red blood cell accumulation in the microaneurysm

lumen

o Rupture produces blot hemorrhages

o May appear yellowish in time as endothelial cells proliferate and

produce basement membrane

Dot and blot hemorrhages

o Occur as microaneurysms rupture in the deeper layers of the

retina such as the inner nuclear and outer plexiform layers.

o Appear similar to microaneurysms if they are small; may need

(13)

Flame-shaped hemorrhages - Splinter hemorrhages that occur in the

more superficial nerve fiber layer.

Retinal edema and hard exudates - Caused by the breakdown of the

blood-retina barrier, allowing leakage of serum proteins, lipids, and protein

from the vessels.

Cotton-wool spots

o Nerve fiber layer infarction from occlusion of precapillary

arterioles

o Fluorescein angiography - No capillary perfusion

o Frequently bordered by microaneurysms and vascular

hyperpermeability

Venous loops, venous beading

o Frequently adjacent to areas of nonperfusion

o Reflects increasing retinal ischemia

o Most significant predictor of progression to PDR

Intraretinal microvascular abnormalities

o Remodeled capillary beds without proliferative changes

o Collateral vessels that do not leak on fluorescein angiography

(14)

CLASSIFICATION OF DIABETIC RETINOPATHY

Early Treatment Diabetic Retinopathy Study [ETDRS]

Levels of Diabetic Retinopathy

Nonproliferative Diabetic Retinopathy (NPDR)

A. Mild NPDR

• At least one microaneursym

B. Moderate NPDR

• Hemorrhages or microaneurysms (H/Ma),hard exudates.

• Soft exudates, Venous beading (VB), and intraretinal microvascular

abnormalities (IRMAs)

• definitely present.

C. Severe NPDR

• H/Ma in all 4 quadrants

• VB in 2 or more quardrants

• IRMA in at least 1 quadrant

D.Very Severe NPDR

• Any two or more of the following

• H/Ma in all 4 quadrants

• VB in 2 or more quardrants

(15)

Proliferative Diabetic Retinopathy

E. Early PDR

• New vessels on the retina

F. High-Risk PDR

• Mild new vessels on the disc (NVD) with vitreous haemorrhage

• Moderate to severe NVD (1/4 to ½ disc area) with or without vitreous

haemorrhage.

• Moderate neovascularisation elsewhere (1/2 disc area) with vitreous

haemorrhage.

Clinically Significant Macular Edema (any ONE

of the following)

• 1. Thickening of the retina located 500 μm or less from the center of the

macula

• 2. Hard exudates at 500 μm or less from the center of the macula with

thickening of the adjacent retina

• 3. A zone of retinal thickening, one disc area or larger in size, any portion

(16)

International Clinical Diabetic Retinopathy (DR) Disease Severity Scale

Proposed Disease Severity Level Findings Observable With Dilated Ophthalmoscopy

No apparent DR

No abnormalities

Mild nonproliferative DR

Microaneurysms only

Moderate nonproliferative DR

More than “mild” but less than “severe”

Severe nonproliferative DR

Any of the following:

20 or more intraretinal hemorrhages in 4 quadrants

Definite venous beading in 2 or more quadrants

Prominent IRMA in 1 or more quadrants and no Neovascularization

(17)

International clinical classification of diabetic retinopathy

Severity of diabetic macular edema

2 major levels, with subcategories for diabetic macular edema

Proposed Classification Findings Observable Upon Dilated Ophthalmoscopy

Diabetic Macular Edema Absent

No retinal thickening or hard exudates in posterior pole

Diabetic Macular Edema Present

Some retinal thickening or hard exudates in posterior pole

If diabetic macular edema is present, it can be categorized as follows:

Proposed Classification Findings Observable Upon Dilated Ophthalmoscopy

Mild Diabetic Macular Edema Some retinal thickening or hard exudates in posterior pole but distant from the macula

Moderate Diabetic Macular Edema Retinal thickening or hard exudates approaching the center of the macula but not involving the center

(18)

Hard exudates are a sign of current or previous macular edema. Diabetic

macular edema is defined as retinal thickening and this requires a

3-dimensional assessment that is best performed by a dilated examination using

slit-lamp bio microscopy and/or stereo fundus photography.

Patients with CSME should be considered for laser surgery. Appropriate

laser photocoagulation surgery reduces the risk of visual loss by more than

50%, compared with no treatment ever. Even in the presence of 20/20 or better

vision, patients with CSME should be considered for laser surgery because

substantial recovery of reduced visual acuity is relatively unusual following

treatment. A minority of patients have improvement in vision. In a majority of

cases, the goal of treatment with laser photocoagulation is to stabilize the visual

acuity. When treatment is deferred, as may be desirable when the center of the

macula is not involved or imminently threatened, patients should be observed

closely (at least every 3 to 4 months) for progression.

The diagnosis of diabetic macular edema can be difficult. Macular

edema is best evaluated by dilated examination using slit-lamp biomicroscopy

and/or stereo fundus photography. An ophthalmologist who treats patients for

this condition should be familiar with relevant studies and techniques as per

the ETDRS.

Effective surgical treatment and retreatment protocols have been

(19)

side effects and risks of treatment. The goal of treatment is to reduce the rate of

visual loss or stabilize visual acuity.

Most patients require more than one treatment session (average: 3-4),

(20)

RISK FACTORS FOR DIABETIC RETINOPATHY

Duration of the diabetes

In type II diabetes , the incidence of diabetic retinopathy increases with

the duration of the disease. Of patients with type II diabetes, 23% have NPDR

after 11-13 years, 41% have NPDR after 14-16 years, and 60% have NPDR

after 16 years.

Glucose control

For patients with non–insulin–dependent diabetes mellitus, the

American Diabetes Association has suggested that glycosylated hemoglobin

levels of less than 7% (reflecting long-term glucose levels) should be the goal

in all patients to prevent or slow down the onset of diabetes-related

complications.

Renal disease, as evidenced by proteinuria and elevated blood urea

nitrogen/creatinine levels, is an excellent predictor of the presence of

retinopathy. This probably is due to the fact that both conditions are caused

by DM-related microangiopathies such that the presence and severity of one

reflects that of the other. Evidence suggests that aggressive treatment of the

nephropathy may have a beneficial effect on the progression of diabetic

retinopathy and neovascular glaucoma.

Systemic hypertension, in the setting of diabetic nephropathy, correlates

(21)

complicate diabetes in that it may result in hypertensive retinal vascular

changes superimposed on the preexisting diabetic retinopathy, further

compromising retinal blood flow.

Proper management of hyperlipidemia (elevated serum lipids) may

result in less retinal vessel leakage and hard exudate formation. The reason

behind this is unclear.

Pregnant women without any diabetic retinopathy run a 10% risk of

developing NPDR during their pregnancy. Of those with preexisting NPDR,

4% progress to the proliferative type.

In the Wisconsin Epidemiological Study of Diabetic Retinopathy

cataract was the most common cause of legal blindness in older- onset

diabetes, and the second most common cause in diabetic patients with

(22)

PATHOGENESIS OF DIABETIC CATARACT

The enzyme aldose reductase catalyzes the reduction of glucose to

sorbitol through the polyol pathway, a process linked to the development of

diabetic cataract.

It has been shown that the intracellular accumulation of sorbitol leads to

osmotic changes resulting in hydropic lens fibers that degenerate and form

sugar cataracts .In the lens, sorbitol is produced faster than it is converted to

fructose by the enzyme sorbitol dehydrogenase. In addition, the polar character

of sorbitol prevents its intracellular removal through diffusion. The increased

accumulation of sorbitol creates a hyperosmotic effect that results in an

infusion of fluid to countervail the osmotic gradient. Animal studies have

shown that the intracellular accumulation of polyols leads to a collapse and

liquefaction of lens fibers, which ultimately results in the formation of lens

opacities.

Furthermore, studies have shown that osmotic stress in the lens caused

by sorbitol accumulation induces apoptosis in lens epithelial cells leading to

the development of cataract.

A study performed by Oishi et al. investigated whether aldose reductase

is linked to the development of adult diabetic cataracts. Levels of aldose

reductase in red blood cells of patients under 60 years of age with a short

(23)

subcapsular cataracts. A negative correlation has been shown in diabetic

patients between the amount of aldose reductase in erythrocytes and the density

of lens epithelial cells, which are known to be decreased in diabetics compared

to nondiabetics suggesting a potential role of aldose reductase in this

pathomechanism.

The polyol pathway has been described as the primary mediator of

diabetes-induced oxidative stress in the lens .Osmotic stress caused by the

accumulation of sorbitol induces stress in the endoplasmic reticulum the

principal site of protein synthesis, ultimately leading to the generation of free

radicals. There are numerous recent publications that describe oxidative stress

damage to lens fibers by free radical scavengers in diabetics. However, there is

no evidence that these free radicals initiate the process of cataract formation but

rather accelerate and aggravate its development. Hydrogen peroxide is elevated

in the aqueous humor of diabetics and induces the generation of hydroxyl

radicals .Furthermore, increased glucose levels in the aqueous humor may

induce glycation of lens proteins, a process resulting in the generation of

superoxide radicals and in the formation of advanced glycation endproducts.

By interaction with cell surface receptors such as receptor for advanced

glycation endproducts in the epithelium of the lens further hydrogen peroxide

is generated.

In addition to increased levels of free radicals, diabetic lenses show an

(24)

The loss of antioxidants is exacerbated by glycation and inactivation of lens

antioxidant enzymes like superoxide dismutases.

In conclusion, a variety of publications support the hypothesis that the

initiating mechanism in diabetic cataract formation is the generation of polyols

from glucose by aldose reductase which results in increased osmotic stress in

(25)

STUDIES REGARDING THE INCIDENCE OF

DIABETIC CATARACT

Several clinical studies have shown that cataract development occurs

more frequently and at an earlier age in diabetic compared to nondiabetic

patients Data from the Framingham and other eye studies indicate a three to

fourfold increased prevalence of cataract in patients with diabetes under the age

of 65, and up to a twofold excess prevalence in patients above 65 .The risk is

increased in patients with longer duration of diabetes and in those with poor

metabolic control. A special type of cataract—known as snowflake cataract—is

seen predominantly in young type 1 diabetic patients and tends to progress

rapidly. Cataracts may be reversible in young diabetics with improvement in

metabolic control. The most frequently seen type of cataract in diabetics is the

age-related or senile variety, which tends to occur earlier and progresses more

rapidly than in nondiabetics.

The Wisconsin Epidemiologic Study of Diabetic Retinopathy

investigated the incidence of cataract extraction in people with diabetes.

Furthermore, additional factors associated with higher risk of cataract surgery

were determined. The 10-year cumulative incidence of cataract surgery was

8.3% in patients suffering from type 1 diabetes and 24.9% in those from type 2

diabetes. Predictors of cataract surgery included age, severity of diabetic

retinopathy and proteinuria in type 1 diabetics whereas age and use of insulin

(26)

A follow-up examination of the Beaver Dam Eye Study cohort,

consisting of 3684 participants 43 years of age and older, performed 5 years

after the baseline evaluation showed an association between diabetes mellitus

and cataract formation . In the study, the incidence and progression of cortical

and posterior subcapsular cataract was associated with diabetes. In addition,

increased levels of glycated hemoglobin were shown to be associated with an

increased risk of nuclear and cortical cataracts.

In a further analysis of the Beaver Dam Eye study the prevalence of

cataract development was studied in a population of 4926 adults . Diabetic

patients were more likely to develop cortical lens opacities and showed a

higher rate of previous cataract surgery than nondiabetics. The analysis of the

data proved that longer duration of diabetes was associated with an increased

frequency of cortical cataract as well as an increased frequency of cataract

surgery.

The aim of the population-based cross-sectional Blue Mountains Eye

Study was to examine the relationship between nuclear, cortical, and posterior

subcapsular cataract in 3654 participants between the years 1992 to 1994. The

study supported the previous findings of the harmful effects of diabetes on the

lens. Posterior subcapsular cataract was shown to be statistically significantly

associated with diabetes. However, in contrast to the Beaver Dam Eye Study,

nuclear cataract showed a weak, not statistically significant, association after

(27)

A population-based cohort study of 2335 people older than 49 years of

age conducted in the Blue Mountains region of Australia investigated

associations between diabetes and the 5-year incidence of cataract. The results

of this longitudinal study conducted by the same group of investigators as the

Blue Mountains Eye Study demonstrated a twofold higher 5-year incidence of

cortical cataract in participants with impaired fasting glucose. Statistically

significant associations were shown between incident posterior subcapsular

cataract and the number of newly diagnosed diabetic patients.

The Visual Impairment Project evaluated risk factors for the

development of cataracts in Australians. The study showed that diabetes

mellitus was an independent risk factor for posterior subcapsular cataract when

present for more than 5 years.

A goal of the Barbados Eye study was to evaluate the relationship

between diabetes and lens opacities among 4314 black participants . The

authors found that diabetes history (18% prevalence) was related to all lens

(28)

CATARACT SURGERY IN DIABETIC PATIENTS

Approximately 10-15% of all patients who undergo cataract surgery

are diabetics.

The 10-year cumulative incidence of cataract surgery in patients

with diabetes in the Wisconsin Epidemiological Study of Diabetic

Retinopathy was two to five times higher than in comparable non diabetic

population Cataract in diabetic patients decreases the visual acuity and

makes an adequate examination as well as photocoagulation of the retina

more difficult or nearly impossible. Therefore, it is necessary and

important to perform cataract surgery for visual rehabilitation and also

for diagnostic and therapeutic reasons. This is also postulated in other

studies.

Nevertheless, patients with diabetes are treated more cautiously.

Some studies have shown that cataract surgery causes progression of

retinopathy with new hemorrhages, exudates, and macular edema. This

progression is also associated with a poor visual outcome in about 1 in

10 patients.

These results have not been confirmed in other studies, however .

Recent studies have found that the principal determinant of the

postoperative visual outcome appears to be the presence or absence of a

(29)

Diabetics with mild to moderate diabetic retinopathy represent a

high proportion of all patients with diabetic changes of the retina. For

this reason, we evaluated visual outcome and disease progression after

cataract surgery in eyes with no or mild to moderate diabetic retinopathy

at baseline and 1 year after surgery.

There has been a recent shift in emphasis towards earlier cataract

extraction in diabetics. Cataract surgery is advisable before lens opacity

precludes detailed fundus examination.

While the overall outcomes of cataract surgery are excellent, patients

with diabetes may have poorer vision outcomes than those without diabetes.

Surgery may cause a rapid acceleration of retinopathy, induce rubeosis or lead

to macular changes, such as macular edema or cystoid macular edema. The

worst outcomes may occur in operated eyes with active proliferative

retinopathy and/or preexisting macular edema.

In diabetics with or without evidence of diabetic retinopathy the

blood-aqueous barrier is impaired leading to an increased risk of postoperative

inflammation and development of a sight-threatening macular edema, a process

that is exacerbated by cataract surgery . Factors that influence the amount of

postoperative inflammation and the incidence of clinical and angiographic

cystoid macular edema are duration of surgery, wound size and posterior

(30)

An analysis of Medicare beneficiaries from the years 1997 through

2001 revealed that the rate of cystoid macular edema diagnosis after cataract

surgery was statistically significantly higher in diabetic patients than in

nondiabetics.

Several clinical studies investigated the role of cataract surgery on the

progression of diabetic retinopathy.

One year after cataract surgery, the progression rate of diabetic

retinopathy ranges between 21% and 32% Borrillo et al. reported a

progression rate of 25% after a follow-up period of 6 months .A retrospective

review of 150 eyes of 119 diabetic patients undergoing cataract surgery

showed a similar progression of diabetic retinopathy in 25% of cases within the

follow-up period of 6–10 months A prospective study evaluating the onset or

worsening of macula edema at 6 months following cataract surgery in patients

with mild or moderate nonproliferative diabetic retinopathy reported an

incidence of 29% (30 of 104 eyes) of macula edema based on angiographic

data. Krepler et al. investigated 42 patients undergoing cataract surgery and

reported a progression of diabetic retinopathy of 12% in operated versus 10.8%

in nonoperated eyes during the follow-up of 12 months . During the same

follow-up period of 12 months, Squirrell et al. showed that out of 50 patients

with type 2 diabetes undergoing unilateral cataract surgery 20% of the operated

eye and 16% of the nonoperated had a progression of diabetic retinopathy. Liao

(31)

mild to moderate nonproliferative diabetic retinopathy 11 eyes (57.9%) showed

progression of diabetic retinopathy 1 year after surgery, while 12 eyes (63.2%)

had progressed 3 years postoperatively. The progression rates were statistically

significant when compared to eyes without preoperative retinopathy.

A recently published prospective study evaluated eyes from 50 diabetic

patients with and without retinopathy after cataract surgery by optical

coherence tomography. The authors reported an incidence of 22% for macula

edema following cataract surgery (11 of 50 eyes) while macula edema did not

occur in eyes without retinopathy. When only eyes with confirmed diabetic

retinopathy were evaluated, the incidence for postoperative macula edema and

cystoid abnormalities increased to 42% (11 of 26 eyes).

Minimal changes from baseline values in center point thickness were

observed in eyes with no retinopathy.

Eyes with moderate nonproliferative diabetic retinopathy or proliferative

diabetic retinopathy developed an increase from baseline of 145microns and

131microns at 1 month and 3 month, respectively. The difference in retinal

thickening between the 2 groups at 1 and 3 months was statistically significant

and among patients with retinopathy inversely correlated with visual acuity

(32)

Influence of diabetes on operative risk and wound healing

The time worn aphorism that postoperative morbidity is higher in

persons with diabetes is not supported by clinical studies. The conventional

postulate that optimal perioperative glycemic control enhances the chances

of successful wound healing in diabetes is supported only by

experimental studies in animal models of diabetes. These studies implicate

hyperglycemia and insulin deficiency as factors contributing to impaired

wound healing. Deficient formation of granulation tissue and collagen, poor

tensile strength of deep surgical wounds and deficient capillary in growth

into the wound have been demonstrated. (8)

Preoperative evaluation

In planning for surgery, attention should be directed towards

ensuring that the general physical condition of the patient is as good as

possible. With the changes imposed by shorter hospital stays, the physician

has little time for careful study and correction of related medical problems

before surgery.

The importance of pre- admission out-patient assessment cannot be

over emphasized as it allows for identification and treatment of potential

(33)

Assessment of cardiac risk

Mortality due cardiovascular disease increases sharply with age and

duration of diabetes. Assessment of cardiac risk is a major focus during the

pre-operative evaluation of the patient with diabetes. Particular attention should be

paid to the history of previous cardiac disease and current cardiac symptoms.

Surgery should be postponed for 3 to 6 months in patients with the history of

recent myocardial infarction.

Assessment of renal disease

Renal disease is common in patients with long standing diabetes.

Caution should be exercised in the use of iodine containing angiographic fluids

and contrast agents as these are well recognized nephrotoxins in patients with

significant renal insufficiency. All patients undergoing such studies should be

kept well hydrated with the additional use of furosemide and mannitol, if

needed, to prevent acute renal damage.

Treatment of hypertension

Hypertension is a common accompaniment of diabetes. All reasonable

efforts should be made to bring the blood pressure under control before

surgery. As a general rule, anti-hypertensive medications are given on schedule

(34)

Diabetes treatment during and after surgery

Management is considered satisfactory when the blood glucose levels in

the peri-operative period range between 120-180 mg%. When peri-operative

glucose values are less than 100%, careful vigilance is necessary to avoid

hypoglycemia. The wide spread availability of capillary blood glucose

monitoring has greatly enhanced our ability to control patient’s blood glucose

level during the peri-operative period.

Type 1 diabetes

Patients with this type of diabetes are a heterogenous group who require

individualization of their treatment plan. Knowledge of a patient’s previous

glycemic control, best determined by the glycosylated haemoglobin (HbA1C)

or fructosamine test, can be of help in determing pre-operative insulin

requirement. Alterations in nutrition, variable glucose infusion rates, surgical

stress and post operative pain and immobility are factors that influence post

operative insulin requirement. For these reasons, insulin is often required

during peri-operative period by the patient with poorly controlled Type II

diabetes who is receiving oral agent.

Type 2 diabetes

Surgical patients receiving oral hypoglycemic agents fall into three

(35)

i) those with good glycemic control-for this group, it is usually sufficient

to administer the oral agents on the morning of surgery. Long acting

agents like chlorpropamide should be stopped 24 hrs before surgery in

favour of a shorter acting sulphonyl urea.

ii) those with poor glycemic control that will improve when infection

clears or steroid therapy is discontinued- this group require insulin

therapy temporarily during the peri-operative period

iii) those who actually require insulin therapy with oral agents having failed

to control hyperglycemia- patients in this group have an absolute need

for insulin therapy.

Dietary management

Individualized dietary prescriptions are recommended for the

hospitalized adult patients with diabetes. Hospitilization is an ideal opportunity

to obtain a nutritional assessment and to assist the patient in developing an

appropriate dietary plan. Dietary management should be based on a sound

(36)

AIM

To study the effect of cataract surgery and other factors on the

visual outcome and progression of diabetic retinopathy using the

nonoperated contralateral eye as the control.

MATERIALS AND METHODS

Monocular cataract surgery was performed in 100 patients who had

the same degree of retinopathy in both eyes preoperatively. Patients were

assigned to 1 of 2 groups as follows: Group A, progression of retinopathy in

the operated eye caused by cataract surgery; Group B, no progression of

retinopathy bilaterally, comparable level of progression in both eyes, or more

progression of retinopathy in the nonoperated eye than in the operated eye. The

differences between the 2 groups in age, duration of and treatment methods for

diabetes, renal function were compared. The 12 months follow-up included

(37)

INCLUSION CRITERIA

1. Patients with type 2 diabetes mellitus with no or mild or moderate

nonproliferative diabetic retinopathy without CSME.

2. Patients with immature cataract in the study eye and patients with

either no cataract or immature cataract in the fellow eye

EXCLUSION CRITERIA

1. pseudophakic patients

2. patients having undergone previous laser treatment.

3. patients with severe NPDR ,PDR

(38)

PROCEDURE

PREOPERATIVE EVALUATION

Systemic evaluation comprised of assessment of diabetic status and

type of antidiabetic medication used. A detailed history of diabetic control

over the past 5 years was elicited to know whether the patient’s glycemic

status was stable, fluctuating or not controlled previously.

The present glycemic control was assessed by referring all patients

who were known diabetic or detected to be diabetic on routine

examination, to the diabetology department and surgical fitness obtained

before doing cataract surgery.

For patients with poor control of blood sugar levels, surgery was

deferred until the diabetic status was stabilized. Assosciated conditions like

hypertension,cardiac status and renal status were given special attention in

all cases while taking history and necessary investigations, if

warranted,were done before taking up the patient for surgery.

A complete ocular examination was performed preoperatively and at the

final checkup. This examination included the determination of best corrected

visual acuity using Snellen charts, applanation tonometry, slitlamp

examination, and retinal biomicroscopy at the slitlamp with a 90D lens.

Fundus examinations were also performed by direct and indirect

(39)

Keratometry and A scan were done and intra ocular lens power

calculated using SRK II formula.

SURGERY

All patients were operated only by a single senior surgeon.

Routine SICS with PCIOL was planned in these patients.

Lid preparation was done with betadine solution.

Bridle suture was applied

Fornix based peritomy was done.

Incision was made about 2mm from the limbus with 11 knife .Scleral

tunnel incision was made with crescent knife.

Entry into anterior chamber was made with the keratome and

viscoelastic material was injected into the chamber.

Continuous curvilinear capsulorrhexis was performed.Can opener

capsulotomy was done in those patients in whom capsulorhexis could not be

performed.

Hydrodissection was performed.

Nucleus was rotated and brought to the anterior chamber and delivered

(40)

Cortical aspiration was done using a 23G simcoe cannula with the

infusion of Ringer Lactate solution.

A complete cortical aspiration was ensured by appreciation of

fundal glow.

Viscoelastic material was injected and capsular bag distended .

The integrity of capsular bag was ensured and then rigid PCIOL

was inserted in the bag.

The cortical remnants and viscoelastic material were aspirated and

anterior chamber formed.

In the event of posterior capsular rent vitrectomy was performed and

anterior chamber IOL was inserted.

Injection subconjunctival gentamycin 10 mg and dexamethasone 0.5mg

was injected at the end and dressing applied.

All patients were treated with systemic antibiotics and

anti-inflammatory drugs.

Topical short acting cycloplegic and antibiotic steroid preparation

(41)

The patient was discharged on the 1st postoperative day if there were

no immediate postoperative complications after doing trial vision, slit lamp

examination, and fundus examination.

Patient showing evidence of maculopathic changes during this

immediate postoperative period were considered to have macular lesions.

They were followed up with FFA periodically and necessary intervention

with laser photocoagulation done at appropriate time.

Postoperatvely all patients were followed up every week for 6 weeks

and then at 12,24,48 weeks. Vision testing with pinhole and glasses slit

lamp examination, fundus examination, and FFA if needed ,were done

during the follow up visits and postoperative diabetic status monitored.

Blood sugar was done during follow up and postoperative diabetic

status monitored. Refraction was done on the 6th postoperative week and

glasses for residual error and near vision correction prescribed.

OUTCOME

Outcome variables included changes of visual acuity, changes of

retinopathy grading as compared to the nonoperated fellow eye, and

(42)

ANALYSIS

AGE DISTRIBUTION

Table 1

Age, Years Number of Patients

41 to49 50 to59 60 to 69 70&Above

12 32 29 11.

0 10 20 30 40

No of patients 41 to 49

50 to 59 60 to 69 70 & above

A g e gr oup AGE DISTRIBUTION

Number of patients

The age of the patients ranged from 41 yrs to 81 yrs, the mean age being

62 years. The maximum number of patients belong to the age group of 50 to

59.12 cases belong to the age group 41-49 which is in accordance to the

studies that diabetes results in presenile type of cataract.

(43)

DURATION OF THE DIABETES IN YEARS

Table 2

No of years No of Patients

Found on admission 9

Less than 2 yrs 13

2 to 5 yrs 42

6 to 10 yrs 16

More than 10 yrs 4

0 10 20 30 40 50

No of years Found on adm ission

Less than 2 yrs 2 to 5 yrs 6 to 10 yrs More than 10 yrs

N o o f p a tien ts

DURATION OF DIABETES IN YEARS

No of Patients

The majority of 42 patients with diabetes for 2 to 5 years had

uncomplicated cataract. This shows that cataract in diabetes occurs even before

the onset of retinopathy.

The mean duration of diabetes at the time of surgery was 5.5 years

(44)

POSTOPERATIVE COURSE OF RETINOPATHY IN OPERATED AND NON OPERATED EYES

Table 3

EYE NO CHANGE PROGRESSION

NO. OF EYES

PERCENTAGE NO. OF EYES

PERCENTAGE

OPERATED 50 59.6 34 40.4

NON

OPERATED

72 85.7 12 14.3

0 10 20 30 40 50 60 70 80 90 no.of eyes (in%)

No change Progression course of DR

Postoperative course of retinopathy

Operated Non operated

During the first postoperative year 50 of the operated eyes (59.5%)

showed ‘no change’ in retinal status and 34 (40.4%) showed ‘progression’of

diabetic retinopathy. The corresponding findings in the control group were 72

(45)

This was comparable to those of Pollock where 61.8% showed ‘no

change’ and 38.2% progressed. The corresponding findings in the control

(46)

PROGRESSION OF RETINOPATHY DURING THE FIRST YEAR AFTER CATARACT EXTRACTION IN OPERATED AND NON OPERATED EYES

Table 4

FOLLOW UP PERIOD

OPERATED EYE( n=34) NON OPERATED EYE(n=12)

NO. OF EYES

PERCENTAGE NO. OF EYES

PERCENTAGE

2weeks- 3 months

17 50 4 33.3

4-6 months 10 29.4 5 41.7

7-12 months 7 20.6 3 25

0 5 10 15 20 25 30 35 40 45 50 no.of eyes (in %)

2wks-3mon 4-6mon 7-12mon duration

progression of retinopathy during the first year after cataract surgery

operated eye nonoperated eye

The operated eyes showed the highest percentage, that is, about 50% of

(47)

This was comparable to the study done by Pollock who showed 60% of

progression from 2 weeks to 3 months.

REFERENCE STUDY

Progression of diabetic retinopathy during the first year after cataract extraction in operated eyes.

Follow-up period No. of eyes progressed (in percentage )

2 weeks - 3 months 60

4 - 6 months 30

7 - 12 months 10

In this study there was maximum progression between the first

2 weeks and 3 months that is,60% and 30% of eyes progressed between

(48)

POSTOPERATIVE COURSE OF DIABETIC RETINOPATHY IN RELATION TO ITS PREOPERATIVE STATUS 0 10 20 30 40 50 60 70 80 90 100

NO DR DR

PREOPERATIVE STATUS N O .O F .C A S ES (i n % NO CHANGE PROGRESSION

POSTOPERATIVE COURSE OF DIABETIC RETINOPATHY IN

RELATION TO ITS PREOPERATIVE STATUS IN THE OPERATED

EYE

Table 5

PREOPERATIVE STATUS NO.OF EYES(n=84) NO CHANGE(n=50) PROGRESSION(n=34)

NO DR 41 36

(87.8%)

5 (12.2%)

DR 43 14

(32.6%)

(49)

0 10 20 30 40 50 60 70 80

NO. OF EYES (IN%)

NO DR DR

PREOPERATIVE STATUS

POSTOERATIVE COURSE OF RETINOPATHY IN RELATION TO ITS PREOPERATIVE STATUS

NO CHANGE PROGRESSION In eyes with no evidence of diabetic retinopathy preoperatively there

was no progression of the retinopathy after cataract surgery in 87.8% of cases

whereas 12.2% of cases progressed.

In eyes with evidence of retinopathy preoperatively there was no

postoperative progression in 32.6% of cases whereas it progressed in 67.4% of

cases.

In a study done by Pollock only 29% of eyes with no evidence of

retinopathy preoperatively progressed whereas 80% of eyes with preoperative

retinopathy progressed after surgery.

(50)

In 71% of eyes with no evidenc of retinopathy preoperatively there

was no change even after surgery whereas only 29% of eyes progressed.

In eyes with evidence of retinopathy preoperatively there was no

(51)

P OS T OP ER A T I VE C OU R S E OF D I A B ET I C R ET I N OP A T H Y I N OP ER A T ED EYE A N D N ON OP ER A T ED EYE

0 5 10 15 2 0 2 5 N O D R T O N P D R

M I L D T O M OD . N P D R M OD . T O S EVER E

N P D R C OU R S E OF D R

NO . O F C ASES (PERC ENTAGE)

N ON OP ER A T ED EYE OP ER A T ED EYE

POSTOPERATIVE PATTERNS OF PROGRESSION OF DIABETIC RETINOPATHY IN OPERATED EYE AND NON OPERATED EYE

Table 6

COURSE OF DR OPERATED EYE NON OPERATED EYE

No.of cases

Percentage No.of cases percentage

No DR to NPDR

(5/84) 5.9 (1/84) 1.2

Mild to Mod.NPDR

(18/84) 21.4 (10/84) 9.5

Mod. To severe NPDR

(11/84) 13.1 (3/84) 3.6

(52)

In eyes with no DR preoperatively there was progression to NPDR in

5.9 % of operated eyes and in 1.2% of the non operated eyes. In the operated

eyes there was aggravation of mild NPDR to moderate NPDR in 21.4% of

eyes whereas in the non operated eyes 9.5 % of eyes had progression from

mild to moderate NPDR. In eyes. There was progression from moderate to

severe NPDR in 13.1% of operated eyes the corresponding figures in the non

operated eyes were 3.6%.

This was similar to the findings by Pollock where the maximum

(53)

REFERENCE STUDY

POSTOPERATIVE PATTERNS OF PROGRESSION OF DIABETIC RETINOPATHY IN OPERATED EYE AND NON OPERATED EYE

COURSE OF RETINOPATHY

OPERATED (no. of eyes in %)

NON OPERATED (no. of eyes in %)

No DR to NPDR 9 4.3

NPDR to NPDR 23.6 7.1

No DR to NPDR NPDR to PDR

5.6 1.4

TOTAL 38.2 12.8

In this study there was postoperative progression in 38.2% of eyes

among which 23.6% of eyes progressed from one stage of NPDR to a

higher stage.

In the non operated eyes only 12.8% of eyes had postoperative

progression of NPDR , 7.1% of which progressed from one form of

(54)

VISUAL ACUITY RESULTS AFTER CATARACT SURGERY IN RELATION TO DIABETIC RETINOPATHY

Table 7

VISUAL

ACUITY

NO CHANGE PROGRESSION

NO DR (n=36) DR (n=14) TOTAL (n=50) NO DR (n=5) DR (n=29) TOTAL (n=34) >=6/12 32 (88.9%) 10 (71.4%) 42 (84%) 3 (60%) 9 (31%) 12 (35.3%) <6/12- 6/36 3 (8.3%) 3 (21.4%) 6 (12%) 1 (20%) 9 (31%) 10 (34.5%) <6/36 1 (2.7%) 1 (7.1%) 2 (4%) 1 (20%) 11 (38%) 12 (35.3%)

In the no change group 84% of operated eyes had visual acuity more

than 6/12 at the end of one year,12% had visual acuity in the range of 6/12 to

6/36 and 4% had visual acuity less than 6/36.In the eyes which had progression

of retinopathy only 35.3% had visual acuity more than 6/12, of 34.5% in the

range of less than 6/12 to 6/36 and 35.3% had less than 6/36 at the end of one

(55)

0 10 20 30 40 50 60 70 80 90

No. of cases(in %)

>=6/12 <6/12-6/36 <6/36

Visual acuity

VISUAL ACUITY RESULTS AFTER CATARACT SURGERY IN RELATION TO DIABETIC RETINOPATHY

NO CHANGE

PROGRESSION

In eyes with no pre-existing retinopathy and no change in postoperative

retinal status a visual acuity of at least 6/12 was achieved in 60% of the cases.

By contrast, a relatively high proportion (38%) of eyes with pre-existing

diabetic retinopathy and postoperative retinal deterioration had poor visual

(56)

REFERENCE STUDY

VISUAL ACUITY RESULTS AFTER CATARACT SURGERY IN

RELATION TO DIABETIC RETINOPATHY

Visual Acuity

No change Progression

NoDR (n=38) DR (n=17) Total (n=55)

NoDR(n=9) DR(n=25) Total(n=34)

>6/12 33 (87%) 12 (70%) 45 (82%) 6 (67%) 7 (28%) 13 (38%) 6/15-6/30 4 (10%) 3 (18%) 7 (13%) 2 (22%) 8 (32%) 10 (29%) <6/30 1 (3%) 2 (12%) 3 (5%) 1 (11%) 10 (40%) 11 (32%)

In eyes with no evidence of diabetic retinopathy and no

postoperative progression of retinopathy status about 87% of eyes had

final visual acuity of more than 6/12 . 70% of eyes with preoperative

retinopathy and no postoperative progression had more than 6/12 visual

acuity.

In eyes with no postoperative progression 13% of eyes had visual

acuity ranging from 6/15 to 6/30 and 5% had less than 6/30 vision

postoperatively.

In the eyes which progressed after surgery 38% had more than 6/12

(57)

INTRAOPERATIVE AND POSTOPERATIVE COMPLICATIONS

Among the intraoperative complications posterior capsular rent was

observed in 4 eyes(4.8%) of cases which had an impact on the postoperative

progression of retinopathy and the final visual status.

Of the early post operative complications, striate keratopathy was more

frequent. It was observed in 16 eyes(19%). Iritis was observed in 10

eyes(12%).

Among the late post operative complications, CME occurred in 8

eyes(9.5% ) and PCO occurred in 18 eyes(21.4%) of patients. Ruiz showed an

incidence of PCO in 41.7% and Pasquier 30%.CME was observed in 32% of

(58)

POST OPERATIVE DIABETIC STATUS

Table 8

Glycemic control No of eyes Percentage

Good 45 53.6

Fluctuating 26 31

Poor 13 15.4

POST OPERATIVE DIABETIC STATUS

Good

Fluctuating

Poor

In all these patients, good glycemic control was seen in 53.6% of

patients. A fluctuating level was noticed in 31% of patients and a poor control

in 15.4% of patients during the post operative period. CME and progression to

retinopathy were more related to the fluctuating diabetic control during the post

(59)

COMPARISON OF CLINICAL FEATURES

Table 9

NO CHANGE (n=50) PROGRESSION (n=34)

Mean age, yr (range) 57.8 (45- 64) 61 ( 49-77)

Mean duration of DM, yr (range)

4.8 10.4

No. of. Patients (%)

Male: female 23:27 16:18

Management of DM:

Diet alone 1 1

Hypoglycemic agents 39 ( 78%) 21 (61.8%)

Insulin 10 (20%) 12 (35%)

Vascular disease:

Hypertension 19 12

Cardiac 6 4

Other diseases: 2 3

There was no significant difference between the ‘no change’ and

‘progression’ group with regard to age, sex and systemic diseases.the mean

duration of diabetes was 4.8 yrs in the no change group and 10.4yrs in the

progression group. Regarding the management of diabetes 78% of patients in

no change group were managed with oral hypoglycemic agents and 20%

were managed with insulin whereas in the progression group 35% of patients

(60)

RESULTS

Of the 100 patients 46 were men and 54 were women.

7 patients lost to follow up. Of the 93 remaining patients cataract

extraction was unilateral in 84 patients and bilateral in 9.Only the unilateral

cases were included in the study.

The mean age at the time of surgery was 62 years (range 41 to 81 years)

and the mean duration of diabetes mellitus was 5.5 years.

During the first postoperative year 50 of the operated eyes (59.6%)

showed ‘no change’ in retinal status and 34 (40.4%) showed ‘progression’of

diabetic retinopathy. The corresponding findings in the control group were

72 eyes (85.7%) and 12 eyes (14.3%) .

In eyes with no evidence of diabetic retinopathy preoperatively there

was no progression of the retinopathy after cataract surgery in 87.8% of cases

whereas 12.2% of cases progressed.

In eyes with evidence of retinopathy preoperatively there was no

postoperative progression in 32.6% of cases whereas it progressed in 67.4% of

cases.

The patterns of progression were similar in the operated and

(61)

In eyes with no DR preoperatively there was progression to NPDR in

5.9 % of operated eyes and in 1.2% of the non operated eyes.

In the operated eyes there was aggravation of mild NPDR to moderate

NPDR in 21.4% of eyes whereas in the non operated eyes 9.5% of eyes had

progression from mild to moderate NPDR.

There was progression from moderate to severe NPDR in 13.1% of

operated eyes and the corresponding figures in the non operated eyes were

3.6%.

In eyes with no pre-existing retinopathy and no change in postoperative

retinal status a visual acuity of at least 6/12 was achieved in 88.9% of the

cases. By contrast, a relatively high proportion (38%) of eyes with pre-existing

diabetic retinopathy and postoperative retinal deterioration had poor visual

results of 6/36 or less.

Among the intra operative complications posterior capsular rent was

observed in 4.8% of cases. Of the early post operative complications, striate

keratopathy was observed in 19% of patients. Iritis was observed in 12% of

patients.

Among the late post operative complications, CME occurred on 9.5%

(62)

Regarding the postoperative diabetic status good glycemic control was

seen in 53.6% of patients. A fluctuating level was noticed in 31% of patients

and a poor control in 15.4% of patients.

Among the operated patients there was no difference between the two

subgroups with regard to sex distribution, mean age, or the presence of

systemic disease. The only significant difference was related to the

management and duration of diabetes mellitus.

The mean duration of diabetes was 4.8% in the ‘no change’ group and

10.4% in the ‘progression’ group Among the ‘no change’ group the diabetes

was controlled by hypoglycemic agents in a greater number of patients(78%),

whereas a greater number of patients whose retinopathy progressed needed

(63)

DISCUSSION

The aims of this study were

(1) to find out if the operated eyes of diabetic patients who undergo

cataract surgery are more prone than non-operated eyes of the same

patients to develop or to show progression of diabetic retinopathy;

(2) to identify the risk factors for postoperative progression of diabetic

retinopathy; and

(3) to follow the course of the disease in this particular group of operated

patients.

To achieve the last objective we attempted to eliminate any factors that

might affect the natural course of the disease postoperatively.

Accordingly, we excluded from the study group eyes with any

additional diseases such as glaucoma or macular diseases other than diabetes,

or eyes treated by laser photocoagulation before or immediately after surgery

for pre existing PDR or severe NPDR or CSME. Thus at the time of surgery

the eyes in our study group presented only with No DR or mild to moderate

NPDR. The differentiation between aphakic or pseudophakic cystoid macular

oedema and diabetic cystoid macular oedema is a major problem. In this

(64)

of the characteristics typical for diabetic retinopathy were observed, regardless

of whether foveal cystoid oedema was present or not.

Thus patients with cystoid macular oedema, but with no evidence of

other characteristics of diabetic retinopathy, were included in the 'no change'

group. Within 12 months of surgery diabetic retinopathy progressed in 40.4%

of eyes that under-went cataract extraction as compared with only 14.3% in

non- operated eyes over the same period (Table 3). The incidence of

progression of diabetic retinopathy in our control group is in line with that

reported by Pollock who studied the course of diabetic retinopathy over a

one-year period in the general diabetic population aged 30 or older at the time of

disease onset.

Since the pre-eminent risk variable for the occurrence of any diabetic

retinopathy is thought to be the duration of the disease, this fact should be

kept in mind when planning cataract surgery for diabetic patients.

Pollock et al also found 9% of operated eyes and 4.3% of non

operated eyes having of new onset of retinopathy in patients who had been

free of retinopathy at the start of the study.In our study only 5% of

operated eyes and 1.2% of non operated eyes had new onset of

(65)

The commonest pattern of progression seen in our study group was

worsening of pre-existing NPDR (Table 6) which was similar to the study

by Pollock et al.

Pollock et al found that progression of retinopathy occurred nearly

four times(7/27) as often in eyes with pre existing retinopathy than

without it. In contrast we found that retinal deterioration occurred nearly six

times (5/29) as often in eyes with preexisting diabetic retinopathy as without it

(Table 5), thus pointing to the pre-existence of diabetic retinopathy as a

possible risk factor for its postoperative progression.

The more frequent deterioration of diabetic retinopathy in our study

group than in nonoperated eyes of this and of other series appears to support

earlier suggestions that removal of the lens may result in a progression of

diabetic retinopathy and/or development of rubeosis iridis, in contrast to the

findings reported by Sebestyen, who observed similar progression of

retinopathy in operated and nonoperated eyes. It is not yet clear how the

removal of the lens may affect diabetic retinal changes in general.

However, with regard to one specific characteristic ofdiabetic

retinopathy - the occurrence of endothelial proliferation and neovascularisation

Williams et al showed that human lens extracts can inhibit endothelial

proliferation. Therefore their removal may induce vascular alterations

(66)

Furthermore they also demonstrated considerable inhibition of

endothelial cell activity in extracts of bovine lens capsule, and suggested that

the presence of an intact lens capsule may inhibit the development of iris

neovascularisation.

Clinical experience seems to support these findings.

Aiello et al found that, following ICCE, patients with or without

background retinopathy were at particularly high risk of developing vitreous

haemorrhage, presumably reflecting progression of the disease to PDR. Alparl

and Pollock et al observed deterioration of diabetic retinopathy in some

diabetic patients following either ICCE or ECCE, with the least progression

occurring in patients who underwent ECCE with IOL implantation in the

capsular bag. Although clinical evidence suggests that ICCE may have a

more deleterious effect than ECCE on the postoperative course of diabetic

retinopathy, the precise role of the posterior lens capsule in reducing

vascular complications after cataract surgery in diabetic patients requires

further investigation.

Of the 34 eyes in our study that showed postoperative retinal

deterioration none progressed to PDR but remained at the non-proliferative

stage, sometimes with postoperative macular oedema, which affected the final

visual results. The visual outcome following cataract surgery in our study

(67)

retinopathy who showed postoperative progression; it should however be noted

that in the progression subgroup, good visual acuity was achieved in 60% of

eyes with preoperative No DR and in 31% of eyes with preoperative NPDR.

The largest subgroup (88.9%) to achieve good visual results consisted

of patients with no preexisting diabetic retinopathy and no change

postoperatively.

The only significant difference in general clinical conditions between

patients with no change in retinal status and patients with postoperative

progression of diabetic retinopathy related to the management of diabetes and

duration of diabetes : more patients in the 'progression' group than in the 'no

change' group were managed by insulin and had longer duration of diabetes.

Other factors which influenced postoperative visual outcome were

the incidence of cystoid macular edema (9.5%) and posterior capsular

opacification (21.4%).

The results of this study clearly indicate that progression of diabetic

retinopathy is not uncommon after cataract surgery, even when the technique

employed is ECCE. Patients with diabetic retinopathy prior to surgery are at

higher risk for progression. Accordingly these patients should be closely

monitored postoperatively for early signs of progression of diabetic

retinopathy and where necessary should be considered candidates for laser

(68)

informed that surgery may have an adverse influence on diabetic retinopathy

and that this may affect the final visual outcome. The preoperative status of

diabetic retinopathy may be a significant prognostic factor for the

(69)

CONCLUSION

Duration of diabetes plays a major role in the development of cataract.

Cataract occurs more frequently in Type II diabetics of longer duration.

A good glycemic control during the perioperative period favourably

influences the post operative visual outcome.

Cystoid macular edema and posterior capsular opacification were the

most frequent postoperative complications.

Eyes with no evidence of diabetic retinopathy preoperatively showed

a significantly higher incidence of no change than of progression in their

postoperative retinal status. In eyes with preoperative non proliferative

diabetic retinopathy the opposite was true: their postoperative retinal status

showed a significantly higher incidence of progression than no change.

The incidence of the various patterns of progression observed one

year after cataract surgery in the study eye with their corresponding incidence

in the control eye showed higher percentage of progression of non proliferative

diabetic retinopathy in both.

There is a significant increase in aggravation of preexisting diabetic

eye status in patients with poor postoperative glycemic control and long

Figure

Table 2

Table 2

p.43
Table  3

Table 3

p.44
Table  4

Table 4

p.46
Table  5

Table 5

p.48
Table  6

Table 6

p.51
Table  7

Table 7

p.54
Table  8 Glycemic control

Table 8

Glycemic control p.58
Table  9

Table 9

p.59

References

Updating...

Outline : DISCUSSION